Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022104 (irritable bowel syndrome)
 8,033 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastrointestinal disorders are common in adolescents. Chronic abdominal pain, lactose intolerance, constipation, and irritable bowel syndrome represent the most common gastrointestinal complaints, while inflammatory bowel disease is the major chronic disorder of concern to clinicians. Gallstones and pancreatitis may also be seen in this age group. The authors describe the diagnosis and treatment of these gastrointestinal disorders.
 ...
PMID:Gastrointestinal Disorders in Adolescents. 1035 Jul 72

Chronic abdominal pain occurs in 17% of children aged 0-14 years with a peak of 33% at the age of 7 years. According to the Rome II criteria abdominal pain disorders can be classified as functional dyspepsia, irritable bowel syndrome, functional abdominal pain, abdominal migraine, and aerophagia. This new classification will hopefully lead to a more careful diagnosis of functional abdominal pain syndromes and to better treatment strategies. A thorough history taking and physical examination are the cornerstone of diagnostic workup in children with chronic abdominal pain. An extensive explanation and reassurance are the basis of an adequate treatment and in the majority of cases this is successful.
 ...
PMID:[Functional childhood gastrointestinal disorders. I. Chronic abdominal pain]. 1286 62

Chronic abdominal pain in children can be dependent from motility disorders. The aim of the work was evaluation the frequency of changes in oesophageal manometry in children with chronic abdominal pain. Manometry studies were performed in 40 children with functional abdominal pain (group A, which was divided into subgroups: A1--functional dyspepsia, A2--irritable bowel syndrome, A3--nonspecific abdominal pain), in 11 children with gastritis (group B) and in 24 children as a control (group C). Disorders of lower oesophageal sphincter (LES) function were observed in 72.5% of group A and 45.5% of group B; transient lower oesophageal sphincter relaxations (TLESR) were noticed in 13.5%. Abnormalities of body function with the features of non-specific oesophageal motility disorders were observed in 62.5% in group A and 54.5% in group B during "dry" swallows and in 47.5% and 18.2% respectively during "wet" swallows. These changes were more frequent in dyspeptic children (85.7%). Statistical differences were established among values of resting LES pressure in analysed groups (group A or B versus group C; p < 0.05). In conclusion we mentioned that in oesophageal manometry abnormalities (LES and body function) were observed in children with functional abdominal pain and with gastritis. Characteristic features can not be defined in each group.
 ...
PMID:[Motility disorders in oesophageal manometry in children with chronic abdominal pain]. 1507 18

Chronic abdominal pain is the most distressing symptom in patients with functional digestive disorders (FDD). IBS is the most common gastrointestinal disorder seen in primary care and gastroenterology practice. IBS is a functional bowel disorder in which abdominal pain is associated with defaecation or a change in bowel habit, with features of disordered defecation and with distension. The underlying pathophysiology of IBS is unknown but a chronic visceral hyperalgesia, in the absence of detectable organic disease, is implicated. The exact location of abnormality of visceral pain processing is not known. Theories of its etiology have range widely from the original view that the disease represents a primary disturbance of gut mucosa to emerging conception of the syndrome as emanating from a complex disordered interaction between the digestive and nervous systems. Several lines of evidence suggest a strong modulatory or etiologic role of the central nervous system in the pathophysiology of IBS. A major advance in the understanding of the central mechanisms of pain processing has evolved from application of functional imaging techniques, as represented by positron emission tomography (PET) and functional magnetic resonance imaging (fMRI). In humans, multiple components are involved in somato-visceral pain processings, including sensory-discriminative components, affective components, and cognitive components. Silverman et al, using PET, were the first to explore neural correlates of abdominal pain induced by rectal distension. If healthy subjects activated the ACC, the IBS patients did not while they presented an activation of the left PFC. These findings were consistent with an IBS model that includes both the exaggerated activation of a vigilance network (dorsolateral PFC) and a failure in pain inhibition network anterior cingulate cortex (ACC). In contrast, Mertz et al., using fMRI, observed that pain led to a greater activation of the ACC than did non-painful stimuli thus arguing for an up-regulation of afferent sensitivity to pain. Using fMRI, we also characterized cerebral loci activated by a rectal distension in healthy volunteers. The activation patterns presented a strong similarity with the central processing of somatic pain. In contrast, in a women predominant population of IBS patients, we did not observed any neuronal activation in locations activated in healthy volunteers (ACC, dorsolateral PFC) while a significant deactivation was observed in the IC and in the amygdala, a limbic structure with a role to assign emotional significance to a current experience related to anxiety and fear. Brain imaging techniques thus appear as useful tools to characterize normal and abnormal brain processing of visceral pain in patients with FDD. Reversal effects of chemical compounds targeting these abnormalities either at a peripheral or a central level should be of interest.
 ...
PMID:Visceral sensitivity perturbation integration in the brain-gut axis in functional digestive disorders. 1507 47

Irritable bowel syndrome (IBS) is the most common chronic gastrointestinal (GI) disorder, affecting about 20% of the world's population. Chronic abdominal pain or discomfort relieved by defecation and associated with altered bowel habits are the mainstay in diagnosis. The pathophysiology of IBS remains unknown. This biopsychosocial disorder involves dysregulation of the nervous system, altered intestinal motility, and increased visceral sensitivity. All of these result from dysregulation of the bidirectional communication between the gut with its enteric nervous system and the brain (the brain-gut axis), modulated by various psychosocial and environmental factors (e.g. infection, inflammation). Numerous neurotransmitters are found in the brain and gut that regulate GI activities, including 5-hydroxytryptamine (5-HT, serotonin) and its 5-HT3 and 5-HT4 receptors. The current approach to IBS patients is based on a positive diagnosis of the symptom complex, exclusion of underlying organic disease, and institution of a therapeutic trial. Traditional symptomatic treatment has included antidiarrheals, laxatives and bulking agents/fiber, low-dose tricyclic antidepressants, antispasmodics for pain, and "alternative" therapies (e.g. psychotherapy, hypnotherapy). The scientific evidence supporting this therapy is limited. Novel approaches include visceral analgesics and serotonin agonists and antagonists. In patients with severe diarrhea, 5-HT3 receptor antagonists (e.g. alosetron) and selective M3-type anticholinergics are indicated, in constipation 5-HT4 agonists (e.g. tegaserod), and in pain alfa2-adrenergics (e.g. clonidine), cholecystokinin antagonists, kappa-opioid agonists (e.g. fedotozine), and neurokinin antagonists; some of these agents are still being investigated. Understanding the brain-gut axis is crucial in the development of effective therapies for IBS.
 ...
PMID:The brain-gut axis in irritable bowel syndrome--clinical aspects. 1517 82

Chronic abdominal pain is a common feature of most functional gastrointestinal disorders in children, including functional abdominal pain (FAP) and irritable bowel syndrome (IBS). FAP can impair a child's life and often leads to significant school absences. Although the underlying mechanism is likely multifactorial, early pain experiences during a vulnerable period in the developing nervous system can cause long-term changes in the brain-gut axis and ultimately may result in altered pain pathways and visceral hyperalgesia. Care providers often feel uncomfortable managing patients with chronic abdominal pain, as the pathophysiology is poorly understood, and limited data exist regarding safety and efficacy of therapeutic options in children. The primary goal of therapy in FAP is to alleviate pain symptoms and to help the child return to normal daily activities. Treatment should be individualized and chosen based on the severity of symptoms, the existence of comorbid psychological disorders, and the impact the disorder has on the child's school attendance and normal functioning. Various psychological interventions, such as cognitive-behavioral therapy, hypnosis, and guided imagery, have been successfully used in children with chronic abdominal pain. Pharmacologic therapies such as H(2) blockers, proton-pump inhibitors, tricyclic antidepressants, and various serotonergic drugs have been used, but good controlled trials are lacking. More studies are clearly needed to investigate the benefits and safety of pharmacologic therapy in children. Newer pharmacologic agents that target specific receptors involved in nociception, stress, and neurogenic inflammation currently are being developed. Future targets for visceral hyperalgesia should not only be aimed at alleviating symptoms but also should include prevention, particularly in cases with a suspected sensitizing event such as neonatal pain and postinfectious IBS.
 ...
PMID:Treatment options for chronic abdominal pain in children and adolescents. 1694 66

Chronic abdominal pain is a common gastrointestinal symptom experienced by patients. We have previously shown that IBS patients with visceral hypersensitivity also have evidence of thermal hypersensitivity of the hand and foot that is reversed by rectal lidocaine jelly. We have also recently developed an animal model of chronic visceral and somatic hypersensitivity in rats treated with intracolonic trinitrobenzene sulfonic acid (TNBS). The objective of the current study was to determine the effects of intracolonic lidocaine on visceral/somatic hypersensitivity in TNBS-treated rats. A total of 20 hypersensitive rats received either 20mg intracolonic lidocaine (n=10) or saline jelly (n=10). In comparison to saline jelly, intracolonic lidocaine jelly reduced responses to nociceptive visceral/somatic stimuli in hypersensitive rats. The effects were present within 5-30 min after administration of lidocaine and lasted for 6h. Lidocaine had no effects on recovered rats or control rats that had originally been treated with intracolonic saline instead of TNBS. Local anesthetic blockade of peripheral impulse input from the colon reduces both visceral and somatic hypersensitivity in TNBS-treated rats, similar to results in IBS patients. The results provide further evidence that visceral and secondary somatic hypersensitivity in a subset of TNBS-treated rats reflect central sensitization mechanisms maintained by tonic impulse input from the colon. This study evaluates the reversal of visceral/somatic hypersensitivity in a subset of TNBS-treated rats with intracolonic lidocaine. This animal model may be used in the future to study the mechanisms of local anesthetic agents applied to the gut to reduce visceral pain.
 ...
PMID:Reversal of visceral and somatic hypersensitivity in a subset of hypersensitive rats by intracolonic lidocaine. 1848 44

Chronic abdominal pain is a common symptom of great clinical significance in several areas of medicine. In many cases no organic cause can be established resulting in the classification as functional gastrointestinal disorder. Irritable Bowel Syndrome (IBS) is the most common of these conditions and is considered an important public health problem because it can be disabling and constitutes a major social and economic burden given the lack of effective treatments. IBS aetiology is most likely multi-factorial involving biological, psychological and social factors. Visceral hyperalgesia (or hypersensitivity) and visceral hypervigilance, which could be mediated by peripheral, spinal, and/or central pathways, constitute key concepts in current research on pathophysiological mechanisms of visceral hyperalgesia. The role of central nervous system mechanisms along the "brain-gut axis" is increasingly appreciated, owing to accumulating evidence from brain imaging studies that neural processing of visceral stimuli is altered in IBS together with long-standing knowledge regarding the contribution of stress and negative emotions to symptom frequency and severity. At the same time, there is also growing evidence suggesting that peripheral immune mechanisms and disturbed neuro-immune communication could play a role in the pathophysiology of visceral hyperalgesia. This review presents recent advances in research on the pathophysiology of visceral hyperalgesia in IBS, with a focus on the role of stress and anxiety in central and peripheral response to visceral pain stimuli. Together, these findings support that in addition to lower pain thresholds displayed by a significant proportion of patients, the evaluation of pain appears to be altered in IBS. This may be attributable to affective disturbances, negative emotions in anticipation of or during visceral stimulation, and altered pain-related expectations and learning processes. Disturbed "top-down" emotional and cognitive pain modulation in IBS is reflected by functional and possibly structural brain changes involving prefrontal as well as cingulate regions. At the same time, there is growing evidence linking peripheral and mucosal immune changes and abdominal pain in IBS, supporting disturbed peripheral pain signalling. Findings in post-infectious IBS emphasize the interaction between centrally-mediated psychosocial risk factors and local inflammation in predicting long-term IBS symptoms. Investigating afferent immune-to-brain communication in visceral hyperalgesia as a component of the sickness response constitutes a promising future research goal.
 ...
PMID:Abdominal pain in Irritable Bowel Syndrome: a review of putative psychological, neural and neuro-immune mechanisms. 2109 82

Chronic abdominal pain accompanying intestinal inflammation emerges from the hyperresponsiveness of neuronal, immune and endocrine signaling pathways within the intestines, the peripheral and the central nervous system. In this article we review how the sensory nerve information from the healthy and the hypersensitive bowel is encoded and conveyed to the brain. The gut milieu is continuously monitored by intrinsic enteric afferents, and an extrinsic nervous network comprising vagal, pelvic and splanchnic afferents. The extrinsic afferents convey gut stimuli to second order neurons within the superficial spinal cord layers. These neurons cross the white commissure and ascend in the anterolateral quadrant and in the ipsilateral dorsal column of the dorsal horn to higher brain centers, mostly subserving regulatory functions. Within the supraspinal regions and the brainstem, pathways descend to modulate the sensory input. Because of this multiple level control, only a small proportion of gut signals actually reaches the level of consciousness to induce sensation or pain. In inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) patients, however, long-term neuroplastic changes have occurred in the brain-gut axis which results in chronic abdominal pain. This sensitization may be driven on the one hand by peripheral mechanisms within the intestinal wall which encompasses an interplay between immunocytes, enterochromaffin cells, resident macrophages, neurons and smooth muscles. On the other hand, neuronal synaptic changes along with increased neurotransmitter release in the spinal cord and brain leads to a state of central wind-up. Also life factors such as but not limited to inflammation and stress contribute to hypersensitivity. All together, the degree to which each of these mechanisms contribute to hypersensitivity in IBD and IBS might be disease- and even patient-dependent. Mapping of sensitization throughout animal and human studies may significantly improve our understanding of sensitization in IBD and IBS. On the long run, this knowledge can be put forward in potential therapeutic targets for abdominal pain in these conditions.
...
PMID:Neuroanatomy of lower gastrointestinal pain disorders. 2457 73

Chronic abdominal pain (CAP) is a prevalent disorder related to functional gastrointestinal disorders (FGIDs). In pediatric setting, CAP is a common presenting problem among children and adolescents ages 2 to 18 years with a median prevalence rate of 12%. It was proposed that CAP is the result of the altered pain sensation due to a dysfunction of the brain-gut axis after a complex interaction among biological, psychological and social factors. Children with CAP experience decrease in quality of life compared to children with identifiable organic disease such as inflammatory bowel disease. Despite treatment, 30% of children with CAP have long-lasting complaints with evidence that CAP is a risk factor for the occurrence of irritable bowel syndrome in adults. Efforts have subsequently been made to standardize the diagnostic criteria and adequate follow-up. CAP is associated with significative impairment with considerable impact on self-reported quality of life. The direct and indirect costs are not known in pediatric population and the access to investigations it's frequent. A more appropriate use of Rome III criteria would allow for a clinical diagnosis. The focus of this article will be to report the updated criteria for the diagnosis, follow-up and treatment of this condition.
 ...
PMID:Current Issues in the Management of Pediatric Functional Abdominal Pain. 2475 36


1 2 Next >>